Evidence map›Paper›PMID 32615282›Full record

ArticleMolecular and cellular endocrinology2020

Reciprocal regulation between GCN2 (eIF2AK4) and PERK (eIF2AK3) through the JNK-FOXO3 axis to modulate cancer drug resistance and clonal survival.

Glowi Alasiri, Yannasittha Jiramongkol, Sasanan Trakansuebkul, Hui-Ling Ke, Zimam Mahmud, Kitti Intuyod, Eric W-F Lam

Open access · hybridAbstract read
In one paragraph

Article in Molecular and cellular endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.7field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. GCN2 regulates paclitaxel-induced neuropathic pain.British journal of pharmacology · 2025
    Article
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  5. BRAFbioRxiv : the preprint server for biology · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Glowi AlasiriDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, W12 0NN, UK.
Yannasittha JiramongkolDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, W12 0NN, UK.
Sasanan TrakansuebkulDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, W12 0NN, UK.
Hui-Ling KeDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, W12 0NN, UK.
Zimam MahmudDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, W12 0NN, UK.
Kitti IntuyodDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, W12 0NN, UK; Department of Parasitology, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand; Cholangiocarcinoma Research Institute, Khon Kaen University, Khon Kaen, 40002, Thailand.
Eric W-F LamDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, W12 0NN, UK. Electronic address: eric.lam@imperial.ac.uk.
Imperial College London · GBHammersmith Hospital · GB

Funding

Cancer Research UK 12011Cancer Research UK C37/A18784Department of HealthMedical Research Council MR/N012097/1
6 · The paper itself

Abstract

Pharmaceutical inhibitors of the endoplasmic reticulum (ER)-stress modulator PERK (eIF2AK3) have demonstrated anticancer activities in combination therapies, but their effectiveness as a single agent is limited, suggesting the existence of possible compensatory cellular responses. To explore the potential mechanisms involved, we performed time-course drug treatment experiments on the parental MCF-7 and drug resistant MCF-7Epi

Indexed as

AdenineAntineoplastic AgentsCell Line, TumorDrug Resistance, NeoplasmeIF-2 KinaseEndoplasmic Reticulum StressEpirubicinFemaleForkhead Box Protein O3Gene Expression Regulation, NeoplasticHumansIndolesMAP Kinase Signaling SystemMCF-7 CellsPaclitaxelProtein Serine-Threonine Kinases7-methyl-5-(1-((3-(trifluoromethyl)phenyl)acetyl)-2,3-dihydro-1H-indol-5-yl)-7H-pyrrolo(2,3-d)pyrimidin-4-amineAdenineAntineoplastic AgentsEIF2AK3 protein, humanEIF2AK4 protein, humaneIF-2 KinaseEpirubicinForkhead Box Protein O3FOXO3 protein, humanIndolesPaclitaxelProtein Serine-Threonine KinasesAKTBreast cancerChemotherapyForkhead transcription factorFOXO3JNK

Identifiers

PMID32615282
PMCPMC7493713
OpenAlexW3040050969

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.